Ebook Bansal diseases of ear, nose and throat: Part 2

Section 4 : Oral Cavity and Salivary Glands

34

Oral Symptoms and
Examination

One must not speak unpleasant truths unnecessarily. By indulging in rude words one’s nature becomes rude.
One loses sensitivity without control over one’s words.
—Holi Mother Sarada Devi

Points of Focus
¯¯ Oral Cavity
 Symptoms: Ulcers, Growth, Pain, Xerostomia,
Excessive Salivation, Dysgeusia, Trismus
 Examination: Findings on examination
 Tongue Depressor
¯¯ Evaluation of Cancer Lesions
 History
 Examination
 Investigations
 Imaging
¯¯ Salivary Glands

For general scheme of case taking and general set up of Bull’s
eye lamp light source and head-mirror see chapter history and
examination in section of basic sciences.

ORAL CAVITY

 Clinical Features

¯¯ Diagnostic Imaging
 Sialography
 Radiosialography
 Ultrasonography
 Computed Tomography
 CT Sialography
 Magnetic Resonance Imaging
 MRI sialography
¯¯ Fine-Needle Aspiration Cytology
¯¯ Clinical highlights

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Symptoms
Patients may come to doctor after observing some findings in their mouth, such as an abnormal growth, coating
of tongue, cleft lip, cleft palate or oroantral fistula. Patient
may see their circumvallate papillae of tongue in the mirror
or feel by finger and develop cancer phobia.

1
2

G. xeros, dry + G. stoma, mouth
Dys, bad, difficult + G. geusis, taste

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Pain: Pain may be referred to the ear. It can occur in any part
of the oral cavity.
Xerostomia:1 Dryness of mouth can result from mouth
breathing, radiotherapy, or generalized lesions of the salivary glands.
Excessive salivation: The common causes of excessive salivation are: ulcers of mouth and pharynx, poor orodental
hygiene, ill fitting denture and iodide therapy.
Dysgeusia:2 Taste buds on the anterior two third of tongue
appreciate sweet, sour and salt tastes. Patient can have
unilateral or bilateral perverted, diminished or loss of taste.
It may be associated with lesions, such as heavily coated
tongue, or injury to chorda tympani or the facial nerve.


366

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Trismus:1 The common causes of difficulty in opening the
mouth, which are related to the local oral cavity are oral
submucous fibrosis, ulcerative lesions, dental abscess (Figs
1 and 2), trauma to mandible or maxilla, and malignant
lesions of buccal mucosa and retromolar trigone.
Other: Other oral cavity complaints include ulcers, swelling,
ankyloglossia, cleft lip, cleft palate, injury, halitosis, toothache and gums swelling and bleeding.

Section 4  w  Oral Cavity and Salivary Glands

Sense of taste: It is highly redundant due to its innervation. It

is nearly impossible to lose all sense of taste.
Taste and flavor: They are usually confused with each other. The
taste includes only the ability to sense sweet, salty, bitter and
sour tastes. Flavor includes both taste and smell (80%). Patients
with taste problems may be having flavor and a smell disorder.

Fig. 2: Trismus in a patient of masticator space abscess

Examination
Examine all the different parts of oral cavity by both inspection, as well as palpation (Box 1). Tongue depressors (Fig. 3) are
used in the examination of oral cavity and oropharynx and are
available in different sizes for children and adults.
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Fig. 1: Masticator space abscess. Tender red swelling extending over ramus of mandible and obliterating subangular
depression

Lips: Lips have an outer (cutaneous), an inner (mucosal)
surface and a vermilion border.
Buccal mucosa: is examined by asking the patient to open
the mouth and then retracting the cheek with a tongue
depressor.
Vestibule of mouth: Examine the complete vestibule of
mouth. Look for not only the change in color but also
change in surface appearance. Parotid duct opening may
be red, swollen and discharging. It can be seen opposite the
crown of upper second molar tooth. Examine the skin of

the cheek because carcinoma of buccal mucosa can invade
the same (Fig. 4).

Box 1: Findings on examination of oral cavity
•• Lips (upper and lower): Swellings, growths, vesicles, ulcers, crusts, scars, unilateral or bilateral clefts
•• Buccal mucosa: Change in color, ulceration, vesicles or bullae (pemphigus), white stria (lichen planus), blanched appearance
with submucosal fibrous bands (submucous fibrosis), leukoplakia, erythroplakia, pigmentation, atrophic change in mucosa,
swelling or growth
•• Opening of parotid duct: Red, swollen, secretions (viral or suppurative parotitis)
•• Gums (upper and lower jaws): Red and swollen gums (gingivitis), ulcerated gums covered with membrane (viral ulcers
or Vincent’s infection), hyperplasia (pregnancy or dilantin therapy), growths (benign or malignant neoplasms of maxilla or
mandible), periodontitis
•• Teeth: Number, tartar, loose teeth, carious, malocclusion (fractures of mandible or maxilla, abnormalities of
temporomandibular joint), impacted last molar
•• Hard palate: Cleft palate, oronasal fistula (trauma or syphilis), high arched palate (mouth breathing in adenoids), swelling
(tumors of palate and nose), bony growth in midline of hard palate (torus palatinus), ulcers/growths (benign or malignant)
•• Tongue: Macroglossia (hemangioma, lymphangioma, cretinism, edema or abscess), ankyloglossia (congenital tongue
tie, cancer tongue or floor of mouth, painful ulcer, abscess), deviation on protrusion (hypoglossal paralysis on the side
of deviation), bald or smooth tongue (iron deficiency anemia, median rhomboid glossitis, geographical tongue), fissures
(Melkersson’s syndrome, syphilis), ulcers (aphthous, traumatic due to jagged tooth or denture, malignant, syphilitic or
tubercular), red/white lesions (leukoplakia, erythroplakia), proliferative growth (malignancy)
•• Floor of mouth: Short frenulum (tongue-tie), scar (trauma or corrosive burn), ulcer (trauma, erosion of submandibular
duct stone, aphthous ulcer, malignancy), swelling (ranula, sublingual dermoid, calculus of submandibular duct, benign or
malignant tumors, Ludwig’s angina)
•• Opening of submandibular duct: Red, swollen, secretions
1

L. fr. G. trismus, a creaking, rasping

367

Fig. 5: Hard palate hemangioma
Source: Dr Amit Goyal, Shillong

Fig. 4: Skin involvement in buccal mucosa carcinoma
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Teeth and gums: Examine gums and teeth of both upper
and lower jaws. Cheeks and lips are retracted with the
help of tongue depressor for examining the outer surface
of gums while tongue is pushed away for examining the
inner surface of gums.
Hard palate: See for any swelling (Fig. 5), ulcer and cleft.
Anterior two-third tongue: Only anterior two-third tongue,
which consists of the tip, dorsum, lateral borders and undersurface, is included in the oral cavity. Tongue should be
examined in its natural position and then patient is asked to
protrude it and move it in different directions (Figs 6 to 11).
Floor of mouth: The floor of mouth consists of the area that
lies under the tongue and two lateral gutters (Fig. 12). The
latter are examined by two tongue depressors that retract
tongue and cheek. The submandibular duct opens on
the summit of raised papilla on either side of the tongue
frenulum. The swellings in the floor of mouth are examined by bimanual palpation, which help in differentiating
between submandibular salivary gland and submandibular

lymph nodes.

Fig. 6: Hairy leukoplakia tongue

Fig. 7: White patches on the dorsum of tongue. Note on the left
side one big patch and two small patches on right side

Chapter 34  w  Oral Symptoms and Examination

Fig. 3: Tongue depressor used in the examination of oral cavity
and oropharynx. Note submucosal cleft palate with bifid uvula


Section 4  w  Oral Cavity and Salivary Glands

368

Fig. 8: Black colored tongue due to the ingestion of iron syrup

Fig. 11: Carcinoma anterior two-third tongue left lateral
margin. Note two separate infiltrative lesions involving tip and
middle one-third tongue

Fig. 9: Tongue bite during chewing food

Fig. 12: Ulcerative lesions involving under surface of tongue
and floor of mouth

Tongue depressor
One blade of Lack’s tongue depressor is slightly bent at the end.

The bent end is used for holding the depressor and supports
the little finger of the examiner. The other blade depresses the
tongue and is used like a lever to depress anterior two-thirds
of the tongue with the fulcrum over the lower teeth.
Caution: Touching of the posterior one third of the tongue usually
leads to the gag reflex and not tolerated by the patient.
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Fig. 10: Glossitis involving bilateral margins of the tongue. A
38-year-old male patient with complaints of burning sensations
on the margins of tongue for 5 days

Uses: It is used for examining the oral cavity and the
pharynx. In addition to the depressing of tongue it can
also be used for:
 Squeezing the tonsil
 Retraction of cheek
 Test for gag reflex
 Checking nasal air blast (cold spatula test)
 Spatula test for suspected case of tetanus


Evaluation of cancer lesions
The diagnosis of oral cancer is primarily clinical and confirmed
by histopathology. A detailed history, physical examination
including palpation (Fig. 13) and investigations should include
the following elements:

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Need for reconstruction: Explore need for reconstruction and
their options, and available free and pedicled flap.
Dental evaluation: Dental evaluation before radiation treatment, prosthodontic evaluation for surgical obturator in
cases of maxillectomy.
Speech and swallowing: Consultation and counseling with
speech and swallowing pathologist.

369

History
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Examination
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Local lesion: Dimension and extension including crossing
midline, adjacent structures involved; fixation to underlying periosteum of mandible (Fig. 14) or maxilla, regional
lymphatic spread

Investigations
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Routine: ECG, X-ray chest (preferably both posteroanterior
and lateral views) and basic laboratory profile, liver profile
in alcoholics
Biopsy: Punch/incisional biopsy of the perimeter of the tumor
including some normal adjacent mucosa confirms the tissue
diagnosis. Areas of necrosis and infection should be avoided
as this tissue may confuse the diagnosis.
Fine needle aspiration cytology: Fine needle aspiration
cytology (FNAC) is indicated in cases of suspicious nodes
in the presence of known primary carcinoma.
Synchronous second primary cancer: Search for synchronous
upper aerodigestive tract cancers. About 15% patients of
the oral cavity cancer have multiple primary cancers, which
are present in the upper aerodigestive tract. Risk factors
(such as smoking and alcohol) are common for all these
cancer sites.
Panendoscopy: It includes bronchoscopy, esophagoscopy
and direct laryngoscopy, and has been advocated by many
in all head and neck cancer patients.

Imaging
They help in knowing the extent of primary tumor and regional
lymphadenopathy.
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Fig. 13: Bimanual palpation of floor of mouth and
submandibular region
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Computerized tomography: CT is best for demonstrating
cortical bone erosion and lymph node metastases.
Magnetic resonance imaging: MRI is best for seeing soft
tissue invasion by tumor and extension into medullary
bone.
orthopantogram: In patients with suspected mandibular
invasion, panorex or orthopantogram facilitates dental
evaluation.
Ultrasound: Abdominal ultrasound detects liver metastasis.
positron emission tomography and Single-photon emission
computed tomography: In stage IV patients, PET and single
photon emission computed tomography identify occult
distant metastasis.

Salivary Glands
Clinical Features

Fig. 14:Carcinoma left lower alveolus (premolar to retromolar region) extending to buccal mucosa, floor of mouth and cheek skin.
Patient is retracting her cheek
1

Surrounding the ear

Parotid1 swelling fills the retromandibular hollow region and
elevates the lobule of ear (Fig. 15). Large swellings involve the
preauricular region also.
„„ Acute painful swelling: An acute painful swelling of the
parotid gland usually indicates an inflammatory process.

Chapter 34  w  Oral Symptoms and Examination

Symptoms: They include changes in the fit of existing
denture, otalgia, oral-dental pain, odynophagia, facial
numbness, trismus, dysarthria, dysphagia, bleeding, halitosis or weight loss.
Personal and past history: Patient is inquired about medications, allergies, medical illnesses, previous surgeries,
tobacco and alcohol use.


Section 4  w  Oral Cavity and Salivary Glands

370

Diagnostic Imaging

Fig. 15: Left parotid swelling in a 10-year-old girl. Note the
infraauricular fullness in the area between the angle of mandible
and mastoid

Acute bacterial parotitis: It usually occurs in association
with sialolithiasis of the parotid gland or in patients
who are elderly, malnourished, dehydrated, or immunocompromised.
 Mumps: Acute viral parotitis is mostly due to mumps.

 Calculus: An obstruction of the Stensen’s duct with
a stone may lead to an acute painful swelling of the
parotid gland.
Bilateral parotid swelling: Sjogren’s syndrome and other
forms of autoimmune parotitis usually present with bilateral
parotid swelling, which may be asymmetrical.
Painless slow growth: The tumors of the parotid gland usually
present as a painless swelling for a long duration and have
a slow growth rate. Patients incidentally notice the appearance and consider it a “recent” lump.
Site and extent of swelling: Benign tumors of the parotid are
commonly located in its tail. They are usually well defined,
nontender and freely mobile. The parotid tumor may be
present either in the superficial or in the deep lobe. Tumors
can arise from the deep lobe or extend from the superficial
to the deep lobe (dumbbell-shaped tumors) in the parapharyngeal space (through the narrow stylomandibular tunnel)
and displace oropharyngeal wall medially.
Rapid increase in size of a longstanding mass: It should raise
the suspicion of malignant transformation. It may be due
to inflammation and cystic degeneration. They are most
commonly associated with Warthin’s tumor.
Metastatic: In cases of parotid mass, ask about a history of
cancer of the scalp or facial skin. Metastasis to the parotid
gland can occur from skin cancer including melanoma.
Malignant: Presence of following features indicate malignancy:
 Facial nerve paresis or paralysis
 Pain
 Fixation of mass to the overlying skin or underlying
structures
 Cervical lymphadenopathy.


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CT and MRI are often used in a complementary fashion when
evaluating lesions in and around bone. Both CT and MRI are
able to detect extrinsic and intrinsic masses of a major salivary
gland and determine whether the mass is well circumscribed
or infiltrating.
„„ CT versus MRI: For salivary gland tumors, gadoliniumenhanced MRI is equal or superior to contrast enhanced CT.
They may even be able to approximate the relative position
of the facial nerve in the parotid gland. The approximate
course of the facial nerve can be estimated on the axial
views because nerve exits the stylomastoid foramen and
curves around the ascending ramus at a distance of about
8 mm.
„„ Indications: They are indicated in following conditions:
 Suspicion of malignancy
 Tumors of deep lobe of parotid or parapharyngeal space
 Tumors of submandibular and minor salivary glands
A small well-defined mass of superficial lobe of parotid does

not need imaging studies.

Sialography
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Indications: It is used in the evaluation of following conditions:
 Radiolucent calculi
 Obstructive disease
 Inflammatory lesions
 Penetrating injuries
 Mass lesions
Contraindications: They include the following:
 Iodine allergy
 Acute sialadenitis
Contrast: Water-soluble media (such as meglumine diatrizoate) is preferred over oil-soluble media.
Technique: The ostium is gently dilated after topical anesthesia. The duct is cannulated and contrast is injected
gently until patient experiences pain. For each gland
(parotid or submandibular), anteroposterior, lateral and
oblique X-rays are taken to eliminate all bony overlapping.
If contrast medium is retained, the abnormalities provide
the diagnosis. Several variations include simultaneous
xeroradiography, use of pneumography with tomography,
secretory sialography and CT sialography.

Radiosialography

This radioactive scanning is most commonly used for parotid
gland. It usually uses technetium. It is used to evaluate parenchymal function and to detect mass lesions. Radioisotope
scanning is of no use in lesions of the ductal system. The scan
should be performed in resting state because uptake in the
parotid is greater.
„„ Findings: In a normal study glands are symmetric. Warthin’s
tumor and rare oncocytoma are the only radiopositive
tumors. Postradiation and chronic sialadenitis show
decreased and delayed uptake.


371

CT scanning and MRI are superior in the evaluation of mass
lesions.

Ultrasonography
Ultrasonography (US) has been found good at distinguishing
glandular from extraglandular masses. Ultrasound is quite good
at delineating space occupying lesions of the major salivary
gland. It differentiates between cystic and solid lesions.
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Fig. 16: Ultrasonography neck showing echogenicity of normal
parotid (P) and submandibular (SM) salivary glands
Source: Dr Ritesh Prajapati, Consultant Radiologist, Anand, Gujarat

Like radioisotope scanning and sialography, US is being
supplanted by CT scanning for the evaluation of masses.

Computed Tomography
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Findings
 Low grade malignant and benign tumors: They tend to
have regular and smooth borders.
 High grade neoplasms: They tend to have irregular
infiltration into the parenchyma (irregular outlines and
diffuse borders) and nodal metastases.
 Pleomorphic adenoma and Warthin’s tumor: They usually
have sharp borders.
Characteristics
 Good for intrinsic and extrinsic parotid masses but of
little use in evaluating generalized parenchymal disease
or ductal architecture.
 Far superior in detecting calculi (Figs 18A and B) and in
evaluating deep lobe and parapharyngeal space lesions.
 Excellent at separating cystic lesions from solid masses
and lymphoma from other neoplastic masses.

CT Sialography

It is found excellent for:
Differentiating intrinsic from extrinsic masses

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Fig. 17: Ultrasonography neck showing echogenicity of normal
sternocleidomastoid (SCM) muscle
Source: Dr Ritesh Prajapati, Consultant Radiologist, Anand, Gujarat

A

B

Figs 18A and B: CT scan neck axial sections showing incidentally
detected left submandibular calculus (A) in a case of right aryepiglottic fold mass (B)
Source: Dr Swati Shah, Professor, Radio-diagnosis, GCRI Medical
College, Ahmedabad

Chapter 34  w  Oral Symptoms and Examination

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Normal gland: The normal gland is of homogenous echo
texture, appearing more echogenic (reflects the fat interspersed within the glandular tissue) than the adjacent
muscle (Figs 16 and 17).
Neoplasms: They are usually hypoechoic to normal glandular tissue.
 Malignant tumors: They have a low reflectivity with
poorly defined borders.
 Pleomorphic adenomas: They have a variable reflectivity
with well-defined borders.

Inflammatory lesions: They have high reflectivity with diffuse
borders.
US-guided procedure: Ultrasonic imaging has been used to
direct needle aspiration of parotid abscesses and localizing
calculi (but less accurate than CT).
Color Doppler ultrasound:
 Malignant tumors: They show a higher grade of vascularity than benign tumors.
 Pleomorphic adenoma: Peripheral vascularity with a
hypovascular center.
Limitations: US is unable to evaluate
 Deep lobe parotid masses,
 Masses obscured by the mandible, and
 Masses with parapharyngeal or retropharyngeal extension.


372

Differentiating benign from malignant parotid neoplasms
Showing the relationship of the mass to the facial nerve and
adjacent bone involvement.
„„ Differentiating superficial from deep lobe tumors
„„ Separating parapharyngeal masses from deep lobe parotid
tumors
Equally good results are seen using intravenous contrast
enhancement.
Malignant and inflammatory salivary gland lesions including
abscesses are enhanced by contrast CT. Calculi are best
detected without contrast material because small blood vessels
may simulate small calculi.

Section 4  w  Oral Cavity and Salivary Glands

Magnetic Resonance Imaging
MRI is excellent at separating adjacent soft tissues. MRI is quite
sensitive to the presence of masses within the gland (outlining
the margins of an intraglandular mass).
„„ Normal appearance: The signal is heterogeneous on the
T1 weighted signal (the variable fat content of the parotid
gland gives it an intermediate to bright intensity). On T2
weighted images also the gland is heterogeneous (because
of the serous secretions and water content of the gland).
Fast T2 weighted MRI with thin sections can accurately
evaluate the ductal architecture.
„„ Abnormalities: They are:
 Pleomorphic adenomas: They usually have a homogenous or heterogenous appearance, showing intermediate to low signal intensity on T1 weighting and
appearing hyperintense on T2 weighting (because of
myxoid tissue) and shows homogenous enhancement
following gadolinium.
 Warthin’s tumors: They demonstrate the microcysts on
T2 weighting.

High grade malignant tumors: They are often hypointense on both T1 and T2 weighted images. MRI is again
good at evaluating the extension of neoplasms beyond
the parotid bed.
 Spread: Contrast enhanced T1 weighted images are
used to see perineural spread, bone invasion and tumor
mapping.
–– At the skull base, where there is abundant fat around
the bony foramina, the hyperintense enhancing
tumors show up quite well.

Limitations:They are:
 Less sensitive to subclinical inflammation and cystic
lesions (such as first arch branchial cleft cysts within
the parotid gland) and not sensitive at all to calcification.


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MRI is unable to distinguish between a benign and a malignant
salivary gland lesion, except in extreme cases (those with
infiltrating borders).

MRI sialography
It assesses the ductal changes in Sjögren’s syndrome.

Fine-Needle Aspiration Cytology
Overall accuracy (sensitivity and specificity) of FNAC in salivary
gland lesions, which can be compared with frozen section
depending on the ability of the pathologists, is around 91.1%.
Cellular elements present in cystic lesions, often allow a definitive diagnosis.
Either ultrasound, CT or MRI, which differentiate solid from
cystic lesions before the needle biopsy, should be used in
conjunction with FNAC.

Clinical Highlights
1.Saliva: 1,000–1,500 ml of saliva is secreted in 24 hours. Major amount of saliva, when salivary glands are not stimulated
is secreted by submandibular glands.

2. Excessive salivation: Some of the causes are oral iodides, poorly fitting denture, ulcers in oral cavity and peritonsillitis.
3.Sialography: It is used to diagnose stones, chronic inflammation and tumors in parotid and submandibular glands. It is
contraindicated in acute inflammation and acute sialectasis.

FURTHER READING
1.Sandu K, Makharia SM. Unusual experience in OSMF. Indian J Otolaryngol Head Neck Surg. 2004;56:65-6.
2. Naik Chetana, Claussen C. Qualitative and quantitative representation of taste disturbances: how we do it by pentagon chart. Indian J
Otolaryngol Head Neck Surg. 2010;62:376-80.


35

Oral Mucosal Lesions

We want that education by which character is formed, strength of mind is increased, the intellect is expanded, and by which one
can stand on one’s own feet.
—Swami Vivekananda

points of focus
¯ introduction

red/White LeSionS

 Laboratory Investigations
 Secondary Herpes Simplex Infection or Recurrent Herpes
Simplex Infection

¯ oraL SubmucouS fibroSiS
 Potential for Malignant Change

¯ hand, foot and mouth diSeaSe

¯ Leukoedema

¯ herpangina

¯ oraL LeukopLakia
 Histopathology
 Potential for Malignant Change
 Molecular Biology
 Management

¯ acute necrotizing uLceratiVe gingiVitiS

¯ oraL hairy LeukopLakia

¯ traumatic uLcerS

¯ oraL Lichen pLanuS

¯ radiation mucoSitiS

¯ chronic diScoid LupuS erythematoSuS

¯ bLood diSorderS

¯ candidiaSiS
 Acute Pseudomembranous Candidiasis (Thrush)
 Chronic Hypertrophic (Hyperplastic) Candidiasis or
Candidal Leukoplakia

 Median Rhomboid Glossitis
 Other Clinical Forms of Candidiasis
476

¯ drug-induced oraL LeSionS

¯ recurrent aphthouS StomatitiS
¯ behçet’S Syndrome
¯ erythema muLtiforme
¯ traumatic (eoSinophiLic) granuLoma

pigmented LeSionS
¯ meLanotic macuLeS
¯ meLanoma

¯ fordyce'S SpotS

¯ amaLgam tattoo
 Lesion and its Site

¯ nicotine StomatitiS

LeSionS of tongue

VeSicuLobuLLouS/uLceratiVe LeSionS

¯ geographicaL tongue

¯ pemphiguS VuLgariS

¯ hairy tongue

¯ mucouS membrane pemphigoid

¯ fiSSured tongue

¯ herpeS SimpLex ViruS
 Primary Herpes Simplex Infection

¯ tongue tie
¯ cLinicaL highLightS


374

introduction
The oral cavity works to keep a person hydrated, nutritionally
healthy and well communicated. It protect upper aerodigestive
tract. Impairment to oral health can lead to malnutrition, infection, impaired communication, pain and an impaired quality
of life. The oral cavity acts as a window into a person’s body as
several systemic diseases manifest initially through oral cavity.
The various oral mucosal lesions are enumerated in the Box 1.
The purpose of this chapter is to provide an overview of the
oral cavity disorders.

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Section 4

w

oral cavity and Salivary glands

red/White LeSionS
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oraL SubmucouS fibroSiS
It is an insidious painless oral cavity disease, which is characterized by juxta epithelial deposition of fibrous tissue that
sometimes even extends to the pharynx. Joshi in 1953 first
described this condition in India. The disease is prevalent (2–5
per 1,000) throughout the Indian subcontinent.

pathology
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etiology
Several factors operate together and cause this disorder. Exact
etiology of this condition is not known but the following factors
have been incriminated:
„ Prolonged local irritation:
 Most of these patients have habit of chewing paan (a
specially prepared leaf), betel nut (sopari) and tobacco.
The hard and rough surface of betel nut causes mechanical irritation. Alkaloids in betel nut (such as arecoline)
cause chemical irritation and stimulate collagen
synthesis and the proliferation of buccal mucosa
fibroblasts. Tannins in betel nut stabilize the collagen
fibrils and render them resistant to degradation by the
collagenase.

 Smoking of cigarettes/Bidies also leads to local irritation.
 Excessive amount of chilies and spices in the daily food
may also be an additional factor.
„ Dietary deficiency: As there occurs recurrent vesicle formation and ulceration of the oral mucosa a dietary deficiency
of iron, vitamins B-complex and A has been proposed.
„ Cell mediated immune process: Some consider it a cellmediated immune reaction to arecoline. Arecanut chewing

causes collection of activated T-lymphocytes and macrophages in subepithelial layers of oral mucosa, which result
in reduced production of antifibrotic cytokines (less collagenase) and increased production of fibrinogenic cytokines
(act on mesenchymal cells and proliferate fibroblasts). These
lead to increased production of collagen.
Localized collagen disease: As the histopathological changes
seen in submucous fibrosis are similar to the collagen
diseases such as rheumatoid arthritis and scleroderma,
some scientists think it to be a localized collagen disorder.
Racial: Disease usually affects Indians or people of Indian
origin living abroad. Sporadic cases are also seen in Nepal,
Thailand, South Vietnam and Sri Lanka.
Genetic: As the disease usually affects Indians and not all
the people who chew paan, sopari and tobacco, some
authorities strongly feel it to be genetic disorder.

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Early cases show polymorphonuclear leukocytes, eosinophils and few lymphocytes while lymphocytes and plasma
cells appear in advanced cases. The higher population of
activated T-lymphocytes mainly T-helper/inducer lymphocytes (minor population of B-cells), macrophages and high
CD4+ and CD8+ lymphocyte ratio in subepithelial tissue

suggest main role of cellular immune response and minor
role of humoral immunity.
There occurs a fibroelastotic transformation of connective
tissues in lamina propria associated with epithelial atrophy,
which is sometime preceded by vesicle formation.
Juxta-epithelial fibrosis occurs with atrophy or hyperplasia
of overlying epithelium, which shows areas of epithelial
dysplasia.

potential for malignant change
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Leukoplakia and squamous cell carcinoma are some time
associated with this condition as the predisposing factors
for all these disorders are common.
The malignant transformation (Fig. 1) has been observed
in 3–7.6% of cases.

clinical features
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Age: Though there is no age bar, the disease mostly affects
20–40 years of age group.

box 1: Oral mucosal lesions
• Red/white lesions: Oral submucous fibrosis, leukoedema, oral leukoplakia, oral hairy leukoplakia, oral lichen planus, chronic
discoid lupus erythematosus, candidiasis, fordyce spots, nicotine stomatitis
• Vesiculobullous/ulcerative lesions: Pemphigus vulgaris, mucous membrane (cicatricial) pemphigoid, primary herpes

simplex infection, recurrent herpes simplex infection, herpes simplex infection, hand, foot and mouth disease, herpangina,
acute necrotizing ulcerative gingivitis, recurrent aphthous stomatitis, Behcet’s syndrome, erythema multiforme, traumatic
(eosinophilic) granuloma, traumatic ulcers, radiation mucositis, blood disorders, drug-induced oral lesions
• Pigmented lesions: Melanotic macules, melanoma, amalgam tattoo
• Systemic diseases: Cardiovascular, endocrine, gastroenterology, neurological, renal, hematological (leukemia,
agranulocytosis, pancytopenia, cyclic neutropenia, sickle cell anemia)
• Collagen-vascular and granulomatous disorders: Sjögren’s syndrome, systemic lupus erythematosus, scleroderma,
dermatomyositis-polymyositis, sarcoidosis, Wegener’s granulomatosis
• Lesions of tongue: Geographical tongue, hairy tongue, fissured tongue, tongue tie


„
„
„
„

„

„

Habits: History of chewing of paan, sopari and tobacco is
almost always present.
Trismus: The majority of the patients present with gradually
progressive painless difficulty in opening the mouth (Fig. 2).
Ankyloglossia: The disease may advance and cause difficulty
in protruding out the tongue.
Soreness and burning mouth: Some patients have soreness
of mouth with constant burning sensation, which worsens
during meals especially of pungent spicy type. In later
stages, patient develops insidious, painless and progressive

trismus and ankyloglossia.
Vesicles/Ulcers: Few patients complain of repeated vesicular
eruption on the palate and pillars. Initially there occurs
patchy redness of mucous membrane with formation of
vesicles, which rupture to form superficial ulcers.
Fibrous bands: The most common sites of white fibrotic bands
(Fig. 3) are soft palate, faucial pillars, retromolar area and buccal
mucosa. In later stages, fibrosis develops in the submucosal
layers along with the blanching of mucosa with loss of suppleness. Fibrosis and scarring, which can be seen and felt has
also been demonstrated in the underlying muscle that lead
to further restrictive mobility of soft palate, tongue and jaw.

375

chapter 35
w

treatment
„

fig. 1: Malignancy of tongue right lateral margin in case of oral
submucous fibrosis
„

Medical
 Local steroids/hylase: Topical injection of steroids, which
may be combined with hylase, into the area of fibrous
bands (injection dexamethasone 4 mg and hylase
1500 IU in one ml intraoral submucosal biweekly at
different sites for 8–10 weeks) is more effective than

their systemic use. This brings significant improvement
in symptoms and relieves trismus.
 Avoidance of irritant factors (areca nuts, pan, tobacco,
pungent foods) is of paramount importance.
 Vitamins and minerals: Treatment of existent anemia or
vitamin deficiencies. Vitamin A, zinc and antioxidants
therapy has shown some beneficial effect.
 Jaw opening exercises: They are encouraged.
Surgical: Number of surgical procedures have been reported
(Box 2) but more common include:
 Surgical incision of fibrous bands: Severe trismus associated with marked fibrous bands can be treated by
surgical excision and grafting. It gives immediate
dramatic improvement in opening of the mouth but
usually results in rebound trismus.
 Lasers have also been used to cut the fibrous bands.
 Coronoidectomy and temporal muscle myotomy.
 Reconstruction: Several types of grafts and flaps have
been tried after cutting the fibrous bands (Box 2).

Leukoedema
„

fig. 2: Oral submucous fibrosis. Severe trismus with 0.73 cm
mouth opening

This common asymptomatic incidental finding is characterized by a diffuse and generalized mild surface opacification
(milky alteration) of oral mucosa (usually buccal) which is a
normal variation of oral mucosa.

oral mucosal Lesions

fig. 3: Oral submucous fibrosis. White fibrous bands
involving soft palate, faucial pillars and retromolar area


box 2: Grafts and flaps tried for reconstruction in the
management of oral submucous fibrosis

376

„

• Bilateral tongue flap
• Nasolabial flaps
• Island palatal mucoperiosteal flap
• Bilateral radial forearm free flap

„
„

Associated diseases: The lesion is some time associated with:
 Submucous fibrosis.
 Hyperplastic candidiasis.
 Plummer-Vinson syndrome.
Sex: Males are affected two to three times more often than
females.
Age: Mostly it is seen in the fourth decade of life.

• Buccal pad of fat graft
• Temporalis fascia graft

clinical features

• Split skin graft

„

„

„

Stretching of mucosa dissipates milky alteration and differentiates it from other white lesions of oral mucosa such as
leukoplakia, hyperkeratotic conditions, white spongy nevus,
homogenous type of lichen planus and hereditary benign
intraepithelial dyskeratosis.
Exact cause is not known but the factors that may have
a role include smoking, alcohol, bacterial infections and
electrochemical interactions.
It does not require treatment but must be differentiated
from leukoplakia.

oraL LeukopLakia
Leukoplakia clinically present as a white patch. It should be
differentiated from other white lesions of oral mucosa such as
leukoedema, lichen planus, discoid lupus erythematosus, white
spongy nevus and candidiasis.

Section 4

w

oral cavity and Salivary glands

„

risk factors
The exact cause is not known but the risk factors include:
„

The incriminating factors, which are seen along with this
lesion, are:
 Tobacco smoking
 Smokeless tobacco: Tobacco chewing
 Alcohol abuse: It is especially harmful if combined with
smoking.
 Areca nut and betel
 Chronic trauma (frictionally-induced hyperkeratosis):
It occurs due to ill-fitting dentures and cheek bites.
This is not a true leukoplakia but frictionally-induced
hyperkeratosis. Reversal occurs on elimination of traumatic influence. Chronic friction trauma does not cause
dysplastic or malignant disease.
– Linea alba: In the buccal mucosa it occurs at the
occlusal line.
– Morsicatio: Lip biting habit can cause a slightly
granular hyperkeratotic surface over labial mucosa.
 Chronic sun exposure (Actinic cheilitis): Patches of leukoplakia interspersed with patchy melanotic pigmentation
may develop along the lower lip vermilion surface.
 Sanguinaria: It is herbal root extract present in some
mouth washes and toothpastes. A translucent to slightly
opaque white keratosis patch with well-defined margin

and smooth surface develops along the upper labial
alveolar mucosa. Reversal occurs on withdrawal of
Sanguinaria product.

„

„

Site: Though the most common sites are buccal mucosa
(especially in India) and oral commissures, it may also be
seen over floor of mouth, tongue, gingivobuccal sulcus
and lip.
Lesion: Widely variable clinical lesions include homogeneous and smooth, focal or diffuse, or heterogeneous and
multifocal with variable texture.
 The white, yellowish or gray surface alteration with illdefined margins. Plaques may be small circumscribed
or extensive and soft or thicker, which feel crusty.
 Surface texture can be finely granular or slightly papillary, ulcerative, erosive, nodular, or verrucous.
Induration: Induration indicates malignant change and
immediate biopsy should be taken.

clinical forms
There are different clinical types of leukoplakia. Nodular and
erosive types have higher incidence of malignant transformation.
„ Homogenous leukoplakia (Thin leukoplakia): There is a
smooth or wrinkled white patch, which is less often associated with malignancy. Macular lesion may gradually
progress to more opaque elevated thickened and furrowed,
leathery or wrinkled appearance (Fig. 4). Some lesions may
disappear over time.
„ Nodular (Speckled) leukoplakia: There occur nodular white
patches with erythematous base (Fig. 5).

„ Erosive leukoplakia (Erythroleukoplakia) presents white
patches, which has erosions and fissures and is interspersed
with red patches (erythroplakia).
Erythroplakia:
 Erythroplakia presents as a bright red velvety red patch
(Fig. 6) or plaque usually over lower alveolar mucosa,
gingivobuccal sulcus and the floor of the mouth.
 The lesion is irregular and clearly demarcated from
adjacent normal epithelium.
 Red vascular connective tissue of the submucosa shines
through the mucosa due to decreased keratinization of
mucosal epithelium.
 Clinically lesion may look like granular and/or interspersed with areas of leukoplakia, which is usually
indistinguishable from erythroleukoplakia type of
leukoplakia.
 Most of the erythroplakia lesions show severe dysplasia,
carcinoma in situ or frank invasive carcinoma. The malignant potential is 17 times higher than in leukoplakia.
 Treatment of this lesion needs excision biopsy either
surgically or CO2 laser and regular follow-up.
„ Proliferative verrucous leukoplakia: This uncommon variant
of leukoplakia is multifocal and persistent and occurs


histopathology
„

„

„

fig. 4: Leukoplakia of buccal mucosa. Smooth and wrinkled
white patches. Macular lesions and more opaque elevated thickened and furrowed with leathery and wrinkled appearance

„

It ranges from hyperkeratosis and acanthosis to dysplasia
(disordered cell growth and architectural distortion) or
carcinoma in situ to invasive squamous cell carcinoma.
The dysplasia is traditionally graded as mild, moderate, or
severe.
Carcinoma in situ shows dysplasia in the entire epithelial
compartment (top-to-bottom effect) or severe epithelial
dysplasia. Cellular atypia, which is component of dysplasia,
refers to abnormal cellular features.
About 25% of leukoplakias show epithelial dysplasia
that may be from mild to severe grades. Higher grade of
dysplasia indicates increased chances of malignant change.
A clinical shift from homogeneous to heterogeneous,
speckled, or nodular form is an indication for rebiopsy.

„
„

„

fig. 5: Leukoplakia tongue anterior two-third lateral margin without induration. Note nodular white patches with erythematous
base

„

Loss of heterozygosity: Loss of heterozygosity (LOH) at 3p
and 9p with additional losses at 4p, 8p, 11q or 17p indicates
33-fold increase in risk of cancer development.
Aneuploidy: Eighty four percent of precancers having aneuploidy develop carcinoma.

management
„

„

„

„

Biopsy: An incisional biopsy (multiple biopsies in extensive lesions) must be taken from suspicious areas (such as
erythematous, granular, ulcerated and indurated) to know
the grades of dysplasia and rule out malignancy.
Benign or minimal dysplasia: Observation or excision.
Spontaneous regression is not uncommon in homogenous
variety if incriminating factors are removed.
Premalignant lesions of moderate to severe dysplasia: Excision.
 Methods of complete removal: Scalpel excision, laser
ablation, electrocautery or cryoablation.
Chemoprevention: It is indicated in treated cases or mild
dysplasia. The agents include retinoids, antioxidants, cyclooxygenase (COX)-2 inhibitors.

oraL hairy LeukopLakia
fig. 6: Erythroplakia tongue. Bright red velvety red patch on the
lateral margin of tongue

more often in women. A thin flat white patch progresses
to leathery thickened and papillary to verrucous quality.
Recurrence rate is high and 70% cases develop squamous
cell carcinoma.

„

„

Etiology: This asymptomatic white lesion of oral cavity,
which is considered to be caused by Epstein-Barr virus, has
a relationship with immunosuppression.
Most common site: Bilateral tongue margins. Less common
sites include dorsum of tongue, buccal mucosa and floor
of mouth.

oral mucosal Lesions

molecular biology

w

Leukoplakia is the most common premalignant oral
mucosal lesion.
The chances of malignant change are from 1–17.5%
(average 5%), which varies according to the site, type and
duration of the lesion and age of the patient.
 Age and duration: More the age and duration of the
lesion greater are the chances of malignant change.
 Site: Leukoplakia of floor of the mouth and ventral

surface of tongue have higher incidence of malignant
change.

chapter 35

potential for malignant change

377


378

„

„

chronic diScoid LupuS erythematoSuS
„
„
„

Oral lesions are similar to those of erosive form of lichen
planus. They are always associated with skin lesions.
Oral lesions consist of circumscribed and little elevated
white patches with surrounding telangiectatic halo.
Malignant change usually occurs in labial lesion near
vermilion border in males. These patients should avoid
bright sunlight by the application of ultraviolet barrier
cream to the lips.

candidiaSiS (moniLiaSiS)
This infection is caused by Candida albicans and has two forms:
thrush and chronic hypertrophic candidiasis.

risk factors

This mucocutaneous immunologic disorder is relatively
common (0.2–2% of population). There occurs T-cell lymphocytic reaction to surface epithelial antigen.

They include following:
„ Systemic: Diabetes, antibiotics, age and immunosuppression.
„ Local: Corticosteroids, xerostomia, heavy smoking and
dentures.

clinical features

clinical features

oraL Lichen pLanuS

„

w

„

Oral lesions may be associated with skin lesions, which
consist of pruritic, purple, polygonal papules that are seen
on the forearms and medial side of thigh.
The multifocal and bilateral nature of lesion differentiates

lichen planus from other oral mucosal disorders.

clinical forms

Section 4

oral cavity and Salivary glands

„

Lesions: Range from macular smoothly textured lesions,
subtle white keratotic vertical streaks to thick corrugated
ridges and shaggy surface.
Diagnosis: Histology and demonstration of Epstein-Barr
virus.
 Histology: Hyperkeratosis and irregular surface projections and irregularities.
 Demonstration of Epstein-Barr virus:
– In situ hybridization
– Southern blot procedure
– Polymerase chain reaction (PCR)
– Ultrastructural study
Treatment: It is not required. Lesion disappears with antiretroviral therapy in HIV.

Oral lesions present in various forms such as reticular, plaque,
atrophic, erosive and bullous. Concomitant presence of various
forms is not uncommon. In cases of erosive lichen planus or
atrophic lichen planus, there is risk of malignant change.
„

„

„

„

Reticular lichen planus: Symmetrical bilateral asymptomatic
buccal lesions often in lower mucobuccal folds are seen in
middle-aged population. White keratotic striae form lace-like
pattern over a normal or erythematous mucosa. Other less
common sites include dorsum and lateral portion of tongue,
gingiva and vermilion surface of lip. No active treatment
except reassurance is required.
Erosive lichen planus: It is characterized by painful ulcer on
the buccal mucosa, gingivae or lateral tongue, which is
surrounded by a keratotic periphery. Treatment consists of
topical steroids.
Atrophic or erythematous lichen planus: Thinned edematous
glossy reddened mucosa with loss of surface keratinization
dominates faint white striae.
Bullous lichen planus: In this rare variant the bullae: Size
range from few millimeters to over 1 cm. They rupture and
result in painful ulceration.

Symptoms range from none to burning, dysgeusia, sensitivity
and generalized discomfort. Odynophagia indicates involvement of pharynx.

acute pseudomembranous candidiasis (thrush)
„
„

„

„

chronic hypertrophic (hyperplastic)
candidiasis or candidal Leukoplakia
This invasive C. albicans infection has high incidence of malignant change.
„

treatment
„
„

Corticosteroids: Topical, intralesional injections and systemic.
Other alternatives: Hydroxychloroquine, azathioprine and
retinoids.

Age: This condition can be seen in infants, children and
adults.
Lesion: Thrush presents as white/gray patches on the oral
mucosa and tongue, which when wiped off, leave an
erythematous mucosa.
Predisposing conditions: Adults are usually affected when
they are either immunocompromised or are dehydrated
and suffering from diabetes, AIDS or some systemic malignancy/taking broad spectrum antibiotics, cytotoxic drugs,
steroids or radiation.
Treatment includes:
 Topical application of nystatin or clotrimazole.
 Systemic antifungal agents are fluconazole, itraconazole
and ketoconazole.

 Management of predisposing condition.

„

Most common site: The lesion mostly affects anterior buccal
mucosa often placed posterior to labial commissure along
the occlusal line. A triangular pattern is seen with its apex
directed posteriorly. Other less common sites include palate
and lateral tongue surface.
Appearance: The dense chalky plaques of keratin cannot be
wiped off. They are thicker and more opaque than noncandidal leukoplakia.


„

Treatment
 Surgery: This condition usually requires excisional
surgery.
 Antifungal: Long-term (many months) antifungal (such
as nystatin, amphotericin or miconazole) therapy
eliminates candidal infection and reduces the risk of
malignant transformation.

median rhomboid glossitis
„

„
„

Oral thrush in adults: The common risk factors are corticosteroid

and broad spectrum antibiotics, pregnancy, diabetes mellitus,
nutritional deficiency and human immunodeficiency virus.

„

fordyce’S SpotS
„

„

The aberrant sebaceous glands may be seen as yellowish
or yellow-brown spots, which shine through the buccal or
labial mucosa.
They are seen equally in both the sexes and are considered
normal.

nicotine StomatitiS
„
„

„

The condition is a misnomer as nicotine is not the cause
of this disease.
In smokers (especially reverse smoking) palatal mucosa
shows pin point red spots in the center of umbilicated
papular lesions, which are due to inflammation of the minor
salivary glands. The openings of the ducts of minor salivary
glands react to the heat of the smoke.
Treatment: Patients are advised to give up the habit of smoking.

clinical features
Upper aerodigestive tract lesions precede skin lesions by
months to years in more than 70% of the patients.
„ Lesions: The initial vesiculobullous lesions produce erosions,
blisters, ulcers and pain that tend to run a chronic course.
In contrast to pemphigoid, pemphigus ulcers heal faster
and without scarring. Healing is followed by formation of
new lesions.
„ Sites: Predominantly oropharynx, soft palate and buccal and
labial mucosa. Erythematous and friable gingival marginal
lesions bleed easily on slightest provocation. They extend
to alveolar mucosa.

diagnosis
Clinical
Histological: Clinically intact mucosa near the pemphigus
ulcer shows separation of suprabasal layer (parabasal and
superficial epithelium) from basal layer of the overlying
epithelium.
3. Direct immunofluorescence examination: Fluorescence of
intercellular space regions with anti-IgG antibody is diagnostic for pemphigus vulgaris.

„
„

treatment
Treatment includes systemic steroids and cytotoxic drugs.
1. Initial treatment: Prednisone 1 mg/kg supplemented by
azathioprine or mycophenolate moftil.

2. Severe cases: Cyclophosphamide in conjunction with plasmapheresis.
3. Recalcitrant cases: Intravenous IgG .

mucouS membrane pemphigoid or
cicatriciaL pemphigoid
This is a heterogeneous cluster of autoimmune subepithelial
disorder.

etiopathology
Autoantibodies of IgG and C3 are directed against the molecular
components of basement membrane zone. Linear deposition
of IgG and C3 at the mucosal basement zone is characteristic.

clinical features

VeSicuLobuLLouS/uLceratiVe
LeSionS

„

pemphiguS VuLgariS
This autoimmune mucocutaneous life threatening disorder is
characterized by intraepithelial cleavage and affects older age
group of 50–70 years.

„

Head and neck sites: Oral mucosa is most commonly involved
followed by ocular (conjunctiva), nasal, nasopharyngeal,
laryngeal and esophageal areas. Keratinized tissue of palatal

and gingival area is more commonly affected than buccal.
Lesions: Patchy distribution of vesicles and bullae and
erythematous features. Bulla filled with clear or hemorrhagic fluid ruptures to form superficial ulceration, which

oral mucosal Lesions

„

Acute erythematous candidiasis
 A painful erythematous lesion on the hard palate can
develop after a course of broad-spectrum antibiotics.
Chronic erythematous/atrophic candidiasis
 This is a type of denture sore mouth which can remain
asymptomatic.
Angular cheilitis
 Fissured, macerated or erythematous lesion involves
angle of mouth (oral commissure) and extends on to
the adjacent skin of the face. Associated staphylococcal
infection may be present.

379

w

other clinical forms of candidiasis
„

Adhesion molecule desmogleins (transmembrane glycoproteins) DSG1 (skin) and DSG3 (oral and oropharyngeal mucosa)
are pemphigus antigens, which are targeted by autoantibodies
of IgG class that are deposited within intercellular space and

produces direct damage to the desmosomes.

chapter 35

The exact cause of this condition is not well understood.
Some believe it to be a persistence of tuberculum impar.
Recent studies have revealed chronic candida infection.
As the name suggests a red rhomboid area, devoid of papillae
is seen on the dorsum of tongue in front of foramen cecum.
The condition is asymptomatic and an incidental finding
and does not need treatment.

etiopathology


are covered with shaggy collapsed mucosa. Intraoral scarring is less frequent than ocular scarring that can lead to
symblepharon, ankyloblepharon, corneal opacification,
entropion and trichiasis.

380

diagnosis
„
„

Section 4

w

oral cavity and Salivary glands

„

Clinical
Histopathology: Separation of mucosal epithelium from
the underlying lamina propria and absence of significant
inflammation. Biopsy should be taken from an area near
the inflamed, erosive, or bullous lesion.
Direct immunofluorescence: Linear IgG fluorescence along
the basement membrane is characteristic.

treatment
„

„
„
„

Mild disease: This includes:
 Dapsone for 12 weeks
 Tetracycline/nicotinamide
Oral mucosa involvement: Topical corticosteroids of
moderate to high potency.
Gingival involvement: Similar to pemphigus, skin lesions may
be absent and treatment consists of steroids.
Severe and rapidly progressive disease: Systemic prednisone
and cyclophosphamide.

herpeS SimpLex ViruS: herpetic gingiVoStomatitiS or oroLabiaL herpeS
The herpes simplex virus infection has two types of clinical

presentation: primary and secondary.

etiopathology
Human herpes simplex virus (HHV-1) binds to keratinocytes
and neurons and result in vesicles and migration of viruses to
nerve ganglion (trigeminal, vagus, dorsal root and sympathetic),
where replication occurs between 2 and 10 days of provocation
of recurrent infection.

fig. 7: Herpetic gingivostomatitis involving perioral skin

Laboratory investigations
Though generally not required as the diagnosis is mainly clinical
following are the valid techniques for confirmation of diagnosis:
„
„
„

treatment
„

primary herpes Simplex infection

„
„
„
„

„
„

„

Prevalence: Affects 60–90% of population. Common in
children and less common in adults.
Spread: Direct contact and saliva of recovering or distantly
infected persons.
Incubation period: It is 5–7 days.
Prodrome (48 hours): Focal mucosal erythema and tenderness.
Lesion: Group of thin-walled, delicate and short-lived clusters of multiple small vesicles which like herpangina rupture
and form ulcers surrounded by inflammation.
Site: Any part of the oral cavity both keratinized and nonkeratinized can be involved.
Marginal gingivitis: Classically gingiva appears erythematous, boggy and tender with wide spread vesicles and
ulcers. The disease can involve oropharynx and perioral
skin (Fig. 7).
Resolution: Clinical resolution occurs within 7–14 days.

Symptomatic and supportive.

Secondary herpes Simplex infection or
recurrent herpes Simplex infection
In recurrent human herpes simplex virus (HHV-1) infection, virus
lies dormant in the trigeminal ganglion. Once reactivated, they
travel along peripheral sensory nerves and involve oropharyngeal mucosa.

clinical features
„

„

Viral isolation and culture.
Cytological analysis of vesicle content.
Serum antibody titers.

„

„
„

Age: It usually affects adults and is milder in form as adults
develop some immunity to herpes virus.
Provocations: Some of the common precipitating factors
are emotional stress, fatigue, fever, pregnancy or immune
deficiency states.
Prodrome: Painful, tingling, or burning with subsequent
vesicles at the site.
Lesions: Pinhead size clustered vesicles occur over erythematous and edematous background. After 1–2 days vesicles
rupture and form tender ulcers and ultimately crusting.
Crusting phase is of 5–7 days. Ulcers heal without scarring.
In immunosuppressed patients ulcers are big and scarring
occurs.

clinical forms
„

Herpes labialis: This is the most common clinical form of
recurrent herpes (Fig. 8). The frequency ranges from 5–23%.
The site of affection is the vermilion border of the lip, skin
vermilion junction and adjacent skin. The site remains same
in repetitive episodes.

„
„

and have a yellow base and red areola around them.
Most common sites: Movable mucosa of the faucial pillars,
tonsils, soft palate and uvula.
Treatment: No special treatment is needed. Ulcers usually
heal by themselves within a week time.

381

acute necrotizing uLceratiVe
gingiVitiS
„
„
„

„

„

etiology
diagnosis
„

„

„

Biopsy: Intraepithelial vesicle (filled with serum and free
floating, virally infected keratinocytes) in association with
mixed inflammatory infiltrate.
Smear preparation by unroofing vesicle: Enlarged infected
keratinocytes with multilobulated viral inclusions (Tzanck
cells).
Viral culture: Vesicular fluid.

treatment
„
„

Topical: Topical docosanol cream and penciclovir cream for
herpes labialis.
Systemic: Immunocompetent adults usually do not require
the specific treatment, which includes acyclovir, 200 mg,
five times in a day for 5 days that helps in cutting down the
course of recurrent herpes labialis.

hand, foot and mouth diSeaSe
In this viral infection, which usually affects children, vesicles
occur not only in oral cavity (palate, tongue and buccal
mucosa) but also on the skin of hands, feet and sometimes
even buttocks.

herpangina
„
„
„

Causatives organism: Coxsackie viral infection.
Age: It mostly affects children.
Lesion: There occurs multiple, small vesicles which rupture
to form small ulcers. These ulcers are usually 2–4 mm in size

The exact etiology is not well understood. The multifactorial
etiology may be at play, include following factors:
„ Autoimmune disease
 Both T-cell mediated and antibody-mediated processes
„ Predisposing factors
 Local physical trauma
 Ultraviolet light
 Psychological stress
 Hormonal influences
 Professional groups
 Higher socioeconomic status
 Nonsmokers and nonusers of smokeless tobacco
„ Diseases having oral aphthous ulcerations
 Crohn’s disease/ulcerative colitis.
 Behçet’s syndrome.
 Celiac disease/nontopical sprue: Malabsorption/Glutensensitive enteropathy.
 Food hypersensitivity: Nuts (walnuts, hazelnuts, Brazil
nuts), spices, tomatoes, and chocolate.
 HIV.
 Nutritional: Hematinic and other deficiency states such
as vitamin B12, folic acid and iron.
 Sweet’s syndrome: Acute febrile neutrophilic dermatosis.
 Periodic fever, aphthous stomatitis, pharyngitis and
adenitis syndrome.

„ Drug-induced aphthous-type oral ulcerations
 Non-steroidal anti-inflammatory drugs
 Beta-blockers
 Potassium channel blockers.

oral mucosal Lesions

recurrent aphthouS StomatitiS
This most common nontraumatic form of oral ulcerative disease
chiefly affects oral and oropharyngeal mucosa.

w

Recurrent intraoral herpes simplex
 Typical: Multiple, small, closely cropped tender erosions
and ulcers occur within the keratinized epithelium of hard
palate and attached gingiva. On the hard palate lesions are
seen unilaterally along the distribution of greater palatine
nerve particularly in the first molar and premolar areas. In
mandibular gingiva also the site of predilection is molar
and premolar regions.
 Unusual presentation: Widely scattered vesicles and
ulcers in association with pain, tenderness and fever
in adults.

„
„

chapter 35

fig. 8: Herpes labialis

Causative microorganisms: Vincent’s infection, anaerobic
fusiform bacilli and spirochete (Borrelia vincentii).
Age: Usually affects young adults and middle-aged persons.
Lesions: Lesion starts at the interdental papillae and then
spreads to free margins of the gingivae. Gingivae become
red and edematous.
Vincent’s angina: Ulcers get covered with necrotic slough.
They can be seen not only over the gingivae but also on
the tonsil.
Diagnosis can be confirmed by smear from the affected area.
Treatment: It includes
 Systemic antibiotics which also cover the anaerobes
(penicillin or erythromycin and metronidazole).
 Frequent mouth washes with sodium bicarbonate
solution.
 Attention to dental hygiene.


382

„

w

oral cavity and Salivary glands

„

Section 4

absence of vesicles differentiate herpetiform ulcers from
herpes ulcerations (Fig. 12).

clinical features
Lesions and their sites: It is characterized by recurrent, painful
and superficial ulcers on the movable mucosa of oral cavity
(lips, cheeks, tongue and floor of mouth) and oropharynx
(soft palate and tonsillar pillars). It spares fixed mucosa
of the hard palate and gingivae. Absence of vesicles and
blistering and involvement of only nonkeratinized mucosa
differentiate it from herpes infection.
Clinical forms: The clinical forms are divided into three
classes: minor, major and herpetiform aphthous ulcers
(Table 1).
 Minor: Most common form. Small multiple ulcers occur
in anterior mouth (Figs 9 and 10).
 Major: Major ulcers are deeply created, very big (2–4
cm) and sharply marginated (Fig. 11). In immunocompromised patients major ulcers are more severe, deeper
and painful and last for longer than 6 weeks time and
may serve as a marker for HIV progression.
 Herpetiform: The disproportionate pain, adult onset and
tabLe 1

differential diagnoses
Aphthous ulcers should be differentiated from recurrent herpes
simplex infection (Table 2).

treatment

„

„
„

Mild and infrequent episodes: Symptomatic treatment.
 Lignocaine viscous helps in relieving local pain.
 Topical application of steroids and cauterization with
10% silver nitrate help many patients.
 Tetracycline (250 mg) dissolved in 50 ml of water four
times a day as mouth rinse and then to be swallowed.
Severe and continuous episodes: Short-term systemic
steroids.
Major ulcers: Intralesional steroids.

Clinical forms of recurrent aphthous stomatitis
Minor aphthous ulcers

Major aphthous ulcers

Herpetiform-type aphthous ulcer

Frequency

Most common (85%)

Less common (10%)

Least common (5%)

Size of ulcer

Up to 10 mm

More than 10 mm

Pinhead to 2 mm

Site of ulcer

Nonkeratinized mucosa of
anterior oral cavity

Posterior oral cavity/oropharynx

Wide spread, rarely keratinized mucosa

Type of ulcer

Central necrotic area
surrounded by red halo

Deep with sharp margins

Shallow crater form

Usually single

Multiple

6 weeks

7–10 days

Number of ulcers Multiple
Duration

7–10 days

Pain

Moderate

Very painful

Moderate

Odynophagia

Usually absent

Present

Usually absent

Healing

Without scarring

With scarring

Without scarring

fig. 9: Minor aphthous ulcers on nonkeratinized labial
mucosa of anterior oral cavity

fig. 10: Minor aphthous ulcers on nonkeratinized mucosa of anterior oral cavity. Small multiple ulcers on tongue, anterior tonsillar pillar and soft palate


behçet’S Syndrome

383

This oculo-oro-genital syndrome is characterized by a triad of:
Aphthous-like ulcers in the oral cavity. The edge of the ulcer
is characteristically punched out.
„ Genital ulcerations.
„ Uveitis.
The syndrome can also involve other systems of the body
such as joints and central nervous system.
„

erythema muLtiforme
Erythema multiforme (EM) is a self-limiting, mucocutaneous
disease of unknown etiology. It is usually associated with either
herpes simplex infection or drug ingestion (antiseizures and
sulphonamides).

They include:
„ Viral infections: Recurrent HHV-1 (strongest and most

common trigger), Epstein-Barr virus, chronic hepatitis C
and parvovirus B19.
„ Drug-induced EM: Antiseizure drugs (carbamazepine and
phenytoin) and sulfonamides are most common. Others
include antibiotics and analgesics.
„ Photosensitivity.

clinical features

fig. 12: Herpetiform aphthous ulcers (very small and multiple)
on nonkeratinized mucosa of soft palate and absence of vesicles

tabLe 2

It has rapid onset and involves skin and/or mucous membranes.
About 25% of patients have only oral lesions. Mucosal and cutaneous bullae or ulceration occur in symmetrical distribution.
„ Oral mucosal lesions
 Lesions: Oral mucosal vesicles or bullae soon rupture
and form irregular size and shape ulcers, which are
covered with pseudomembrane (fibrinous plaque) and
bleed easily.

Differentiation between recurrent intraoral herpes simplex and recurrent aphthous stomatitis
Recurrent intraoral herpes simplex

Recurrent herpetiform aphthous stomatitis

Cause

HHSV I/II

Exactly not known

Ultraviolet light and foods

No relation

Triggers

Mucosa involved

Keratinized

Nonkeratinized

Prodrome

Common

Uncommon

Vesicle phase

Present

Absent

Pain

Relatively less

Disproportionately greater

Biopsy

Viral cytopathic effect

Nonspecific

Treatment

Antiviral (topical and systemic)

Steroids (topical and systemic)

oral mucosal Lesions

triggers

w

fig. 11: A major aphthous ulcer. Deeply crated very big ulcer
with sharp margins involving right anterior tonsillar pillar and soft
palate

The disease may be acute (more common), self limiting or chronic,
mild or severe, mucosal, cutaneous or both. It can have overlapping spectrum of following three degrees:
1. EM minor: Self limited, mild disease of skin with minimal
oral involvement.
2. EM major or Stevens-Johnson syndrome (SJS): Fulminant,

progressive, epithelial necrosis of skin and mucosa.
3. Toxic epidermal necrolysis (TEN).

chapter 35

types




384

Site: Any part of oral mucosa can be involved but the
common sites are lips, buccal mucosa and tongue.

Diagnostic feature: Hemorrhagic crusts on the vermilion portion
of lips with edema and severe tenderness are the distinctive
feature.

Oral and oropharyngeal dysfunctions: Sialorrhea, pain,
odynophagia, dysarthria, inability to chew and swallow.
Other mucosal sites
 Eyes, genitalia, esophagus and pulmonary tract.
Skin lesions
 Target or iris lesions (concentric erythematous to
pigmented patches) on the palms, soles and extensor
surfaces of the extremities can be seen if the skin is
involved.

„

radiation mucoSitiS
„


„

„

In the absence of iris or target lesions, other mucocutaneous
diseases (severe aphthous stomatitis, pemphigus, pemphigoid
and erosive lichen planus) should be ruled out. If necessary,
biopsy should be taken.

„

treatment

„

„
„

w

„
„

„

Specific treatment is controversial.
Symptomatic treatment: Analgesics, oral hygiene, bland
mouth rinses, topical steroids, antifungal, and anesthetics.
Short-course of corticosteroids: In EM minor cases as the
disease is self limiting.
Antivirals: In cases of prior HHV-1 infection.

„

„

„

Acute leukemia: Acute lymphoblastic leukemia occurs in
young children while acute myeloid leukemia affects middle
aged or elderly people. It can cause hypertrophy of gums
with ulceration and bleeding.
Agranulocytosis: It may present as ulcerations in throat with
severe neutropenia.
Cyclical neutropenia (periodic falls in neutrophil count):
Patients are prone to infections and oral ulceration.
Pancytopenia: There occurs a drop in RBC count, white cell
count and platelets. CBC and peripheral blood films usually
indicate the diagnosis, which further needs the study of
bone marrow aspiration.

drug-induced oraL LeSionS
„

traumatic (eoSinophiLic) granuLoma

Etiology: Though it is said to be due to deep mucosal injury,
many consider it of unknown etiology as these patients
never have an event of trauma.
Lesion: It is characterized by benign, large (1–2 cm), selflimiting and chronic (weeks to months) oral painful ulcer,
which occurs in and after fifth decade of life. Ulcer has
craterform center, sharp margins and milky white firm
periphery.
Site: This rapid onset ulcer usually develops along the lateral
and ventral surface of tongue. Occasionally, ulcer may be
seen on the dorsum of the tongue.

Radiation therapy can affect the oral and pharynx mucosa.
The mucosa initially becomes red and later on forms spotty
areas of mucositis which coalesce to form large ulcerated
areas that are covered by slough.
Mucositis of cancer chemotherapy (such as methotrexate,
5-fluorouracil and bleomycin) manifests as erythema,
edema and ulceration.

bLood diSorderS
„

differential diagnoses

Section 4

oral cavity and Salivary glands

„

A tablet of aspirin, kept against a painful tooth to get relief
from toothache may lead to aspirin burn, which is seen in
the gingivobuccal sulcus.

„

Drugs like penicillin, tetracycline, sulfa drugs, barbiturates
and phenytoin may cause erosive, vesicular or bullous
lesions in the oral cavity.
Contact stomatitis can also occur due to local reaction to
mouth washes, lozenges, chewing gum, tooth paste or to
prosthetic dental materials. Oral lesions vary from erythema
to vesicles and bullae formation.

pigmented LeSionS
Benign pigmented lesions (Fig. 13) have the potential of
changing into malignant melanomas. About one-fourth of
mucosal melanomas resemble benign lesions therefore biopsy
becomes mandatory.

treatment
„
„
„

Observation.
Topical or intralesional corticosteroids.
Excisional biopsy.

traumatic uLcerS

„
„
„
„

An ulcer on the lateral border of tongue may be due to
jagged tooth or ill-fitting denture.
Cheek bite causes ulcer on the buccal mucosa.
Injury with a pencil or tooth brush can lead to ulcer on the
palate.
Accidental ingestion of acids or alkalis or hot fluids presents
with acute ulcerative lesions of oral and oropharyngeal
mucosa.

fig. 13: Benign pigmented lesion buccal mucosa. Macular zone
of homogeneous hyperpigmentation with well-defined margins


meLanotic macuLeS
The most common sites are the vermilion portion of lower
lip (30%) and gingiva and alveolar mucosa (23%). Other sites
include buccal (16%) and labial mucosa (9%).

„
„

„

Discrete uniformly pigmented macules.
Mucosal melanotic macule: About 10 mm macular zone

of homogeneous hyperpigmentation with well-defined
margins. Focal melanosis (smoker’s melanosis) present over
buccal mucosa as scattered macular evenly pigmented
patches.
Mucosal melanotic nevi: Macular to papular hyperpigmented
lesions can appear in young or at birth.

„

Excisional biopsy.

meLanoma

oral mucosal Lesions

treatment
„

Extent of surgical excision depends upon the depth, size
and site of the melanoma.

prognosis
„

The prognosis is poor. Five year survival rate is 15%.

amaLgam tattoo
This is an extrinsic pigmentation of oral mucosa which occurs
due to traumatic implantation of dental silver amalgam into
neighboring oral mucosa.

fig. 14: Geographical tongue. Note the erythematous area that
is devoid of papillae and surrounded by an irregular keratotic
white outline

Lesion and its Site
„

Well defined, macular grayish-black focal usually 4 mm size
(1 mm to 1.5 cm) mucosal discoloration in lower jaw gingiva,
mucobuccal fold or buccal mucosa.

treatment
„

Simple surgical excision.

LeSionS of tongue
geographicaL tongue or migratory
gLoSSitiS
„

This asymptomatic condition is characterized by erythematous area, which is devoid of papillae and surrounded by an
irregular keratotic white outline (Fig. 14).

w

Oral mucosal melanoma is a rare neoplasm.
„ The most common sites are hard and soft palate (40%) and
gingiva (30%).

„ Preexisting melanosis presents lateral spread or superficial
spreading melanoma in adults. Initially the lesion is heterogeneously pigmented and flat with irregular margin. As
it increases in surface area, the degree of pigmentation
increases to deeper brown to gray-brown.
„ Nodular melanoma arises ab initio as a rapidly growing
nodule.

It may be congenital or acquired.
Acquired: It may be due to syphilis, deficiency of vitamin B
complex or anemia.
„ Congenital: In Melkersson Rosenthal syndrome, congenital
fissuring of tongue (scrotal tongue) is associated with recurrent attacks of facial palsy.
„

chapter 35

„

„
„

Clinical Features: The excessive formation of keratin causes
elongation of the filiform papillae on the dorsum of the
tongue. Due to chromogenic bacteria, they look like brown
or black color hair.
Smoking: It could be one of the factors.
Treatment
 Scraping of the lesions with a tongue cleaner.
 Application of half strength hydrogen peroxide.
 Improving the general nutritional status by vitamins.

 Smoking is prohibited.

fiSSured tongue (fig. 15)

treatment

385

hairy tongue

Lesion
„
„

The shape of lesions keeps on changing.
It does not require any treatment.

fig. 15: Fissured tongue


386

tongue tie (ankyLogLoSSia)
A mobile tongue helps not only in speech but also in maintaining orodental hygiene. It cleans the debris and prevents
formation of dental plaques.
„ True tongue tie, which produces symptoms, is not common.

„

Once the tongue can be protruded beyond the lower incisors it should not cause speech defects.

Treatment: Thick significant tongue tie needs transverse
surgical release with vertical closure. Thin mucosal fold is
simply incised.

Section 4

w

oral cavity and Salivary glands

clinical highlights
1. fordyce’s spots: They represent normal variants of ectopic sebaceous glands. Fordyce’s spot present as granules in
oral cavity.
2. precancerous lesions: Oral lesions having malignant potential are erythroplakia (erythroplasia), leukoplakia, lichen
planus and submucous fibrosis.
3. Wickham’s striae: It is a feature of lichen planus.
4. Leukemia: Oral findings include pale mucous membrane, gingival hypertrophy and petechial hemorrhages.
5. hand, foot and mouth disease: It is caused by Coxsackie A virus.
6. hiV: Oral manifestations include oral candidiasis, hairy leukoplakia and recurrent aphthous ulcers.
7. taste buds: They are in highest number (250) in circumvallate papillae and least (1–18) in fungiform papillae. There are
practically no buds in filiform papillae. Foliate papillae have second highest number (100) of taste buds.

further reading
1. Management submucous fibrosis of oral cavity. Reader’s Forum-21. Indian J Otolaryngol Head Neck Surg. 2000;52:328.
2. Purohit JP, Sharma VK, Singh PN. Leukoplakia: correlative study of clinical picture and cytohistopathology. Indian J Otolaryngol Head
Neck Surg. 2000;52:33-6.
3. Raina C, Raizada RM, Chaturvedi VN, et al. Clinical profile and serum beta-carotene levels in oral submucous fibrosis. Indian J Otolaryngol
Head Neck Surg. 2005;57:191-5.
4. Ramadass T, Manokaran G, Pushpala SM, et al. Oral submucous fibrosis-new dimensions in surgery. Indian J Otolaryngol Head Neck
Surg. 2005;57:99-102.

5. Sandu K, Makharia SM. Unusual Experience in OSMF. Indian J Otolaryngol Head Neck Surg. 2004;56:65-6.
6. Talsania JR, Shah UB, Shah AI, et al. Use of diode laser in oral submucous fibrosis with trismus: prospective clinical study. Indian J
Otolaryngol Head Neck Surg. 2009;61:22-5.
7. How do you treat recurrent Aphthous stomatitis? Reader’s Forum-17. Indian J Otolaryngol Head Neck Surg. 2000;52:201-2.


36

Disorders of Salivary Glands

We need to have three things: the heart to feel, the brain to conceive, the hand to work. Make yourself a dynamo. If you are pure,
if you are strong, you, one man, are equal to the whole world.
— Swami Vivekananda

points of focus
¯ introduction

neoplaSmS of SaliVary glandS

inflammatory diSorderS

¯
¯
¯
¯
¯
¯
¯
¯
¯

¯
¯
¯
¯

¯ mumpS
¯ acute SuppuratiVe SialadenitiS
¯ parotid abSceSS
¯ neonatal SuppuratiVe parotitiS
¯ recurrent parotitiS of childhood
¯ chronic SialadenitiS
 Benign lymphoepithelial lesion
 Kuttner’s tumor
¯ tuberculouS mycobacterial diSeaSe
¯ nontuberculouS mycobacterial diSeaSe
¯ actinomycoSiS
¯ cat Scratch diSeaSe

hiStogeneSiS of neoplaSmS
pleomorphic adenoma
Warthin’S tumor
oncocytoma
hemangioma
lymphangiomaS
mucoepidermoid carcinoma
adenoid cyStic carcinoma
acinic cell carcinoma
SquamouS cell carcinoma
malignant mixed tumor
adenocarcinoma

lymphoepithelial carcinoma

¯ toxoplaSmoSiS

xeroStomia

¯ hiV-aSSociated SaliVary gland diSeaSe

¯ SjÖgren’S Syndrome

obStructiVe diSorderS

¯ diffuSe infiltratiVe lymphocytoSiS Syndrome

¯ SialolithiaSiS

¯ frey’S Syndrome
¯ clinical highlightS

introduction
Salivary gland disorders can be broadly divided into following
categories:
„ Congenital
„ Inflammatory
„ Obstruction and trauma
„ Neoplasms
„ Degenerative conditions

Congenital disorders, which include aplasia/agenesis,
ductal atresia, fistula and ectopic salivary tissue, are rare.

inflammatory diSorderS
mumpS
Mumps is derived from Danish word “mompen” that means
mumbling like an old man, which occurs in mumps due to
pain and trismus.


388

„

Mumps is an acute viral parotitis, which is caused by the paramyxovirus (RNA virus). Other viruses, which can cause acute
viral parotitis, are: coxsackie viruses A and B, enteric cytopathic
human orphan virus, cytomegalovirus and lymphocytic choriomeningitis virus.

complications

epidemiology
„
„

oral cavity and Salivary glands

„
„

„

„

„

It is the most common cause of nonsuppurative acute sialadenitis. It mostly affects children.
Mumps is highly contagious.
The peak incidence occurs in the spring in temperate
climates (little variation in tropics).
The paramyxovirus is endemic in the community. It is
disseminated by means of airborne droplets from salivary,
nasal and urinary secretions.
This paramyxovirus enters through the upper respiratory
tract and then localizes in glandular and central nervous
system tissue.
It has an incubation period of 2–3 weeks.
Viral infection of salivary glands may be locally asymptomatic. The transmission from blood to saliva occurs without
localizing signs in many systemic viral infections such as
rabies, hepatitis, influenza and poliomyelitis.

clinical features

w

„

Section 4

Dietary modifications to minimize glandular secretory
activity.
Fever usually subsides before the resolution of glandular
edema, which may take several weeks.

etiology

„
„
„
„

„

Viral prodome: Low-grade fever, headache, myalgia,
anorexia, arthralgia and malaise just before parotid swelling.
Mumps is characterized by localized pain, which is exacerbated by chewing.
Parotid gland swelling is tense and firm.
Painful swelling of the gland causes displacement of the
pinna, otalgia, trismus and dysphagia.
There is bilateral parotid gland swelling in 75% of cases
but submandibular gland might be affected in rare cases.
Usually one side parotid will swell first followed by enlargement of the other gland in 1–5 days.
The overlying parotid skin is stretched with a glazed appearance, but there is usually no erythema or warmth.

Orchitis, aseptic meningitis, pancreatitis, nephritis and sensorineural hearing loss.

prevention
Subcutaneous injection of vaccination (live attenuated
Jerry Lynn vaccine), usually in combination with measles
and rubella vaccines is given after 12 months of age. The
antibodies produced by vaccine, persist for at least 5 years.
The vaccine is contraindicated in pregnancy, immunocompromised states and allergies to neomycin.

acute SuppuratiVe SialadenitiS

The parotid is most commonly involved salivary gland. The
parotid gland’s serous saliva, unlike mucinous saliva of other
salivary glands, is deficient in lysosomes, IgA antibodies and
sialic acid, which have antimicrobial properties. The saliva from
other glands (submandibular and sublingual glands) contains
high molecular weight glycoproteins that competitively inhibit
bacterial attachment to the epithelial cells of the salivary ducts.

predisposing factors
„
„
„
„
„
„

„

Age: It usually affects 50 and 60 years old people (equal
incidence among men and women).
Debilitating conditions: Malignant lesion and pre-existing
infection.
Postoperative period: Major abdominal and hip repair surgery.
It occurs within the first two postoperative weeks.
Local: Stenosis and sialolithiasis.
Systemic diseases: Diabetes mellitus, hypothyroidism, renal
failure and Sjögren’s syndrome.
Dehydration or significant hemorrhage: The retrograde
bacterial contamination of the salivary ducts from the
oral cavity occurs due to the stasis of salivary flow. It is

secondary to dehydration or significant hemorrhage.
Medications.

investigation
„

„
„

Viral serology: Complement fixing soluble (S) antibodies
against the nucleoprotein core of the virus is associated with
active infection and their levels peak at 10 days to 2 weeks
and disappear within 8–9 months. A fourfold increase in
antibody titer is diagnostic for acute infection. Complement
fixing viral (V) antibodies against outer surface hemagglutinin appear later than S antibodies and persist at low
levels for many years.
A leukocyte count may show leukopenia.
There is an elevation in the serum salivary type amylase.

causative microorganisms
„
„

„

clinical features
„

treatment
Supportive measures include

Bed rest
Oral hygiene
Hydration

„
„
„

Penicillin resistant Staphylococcus aureus in hospitalized
patients.
Streptococcus pyogenes, Streptococcus viridans, Streptococcus
pneumoniae and Haemophilus influenzae (communityacquired cases).
Anaerobic bacteria: Peptostreptococcus, bacteroides species
and fusobacterium.

„
„

It usually presents with rapid onset of pain and swelling over
the affected salivary gland, fever, chills and malaise.
Dehydration with dry mucous membranes and local tenderness, warmth and induration.
Bimanual palpation results in suppurative discharge from
the duct orifice.


investigations
„
„

„

Leukocytosis with neutrophilia and normal serum amylase.
Computed tomography (CT) or ultrasound (US) is indicated
to look for abscess formation if patient does not respond
to medical treatment.
Cultures of purulent drainage from the duct orifice.
Percutaneous needle aspiration limits the amount of
contamination.

parotid abSceSS
„

Usually the diagnosis is apparent. Differential diagnoses
include lymphoma, Bezold’s abscess, cervical adenitis, dental
abscesses presenting as buccal or masseteric space abscesses,
infected branchial cleft or sebaceous cysts.

Multiple small abscesses may coalesce and form large
abscess in an advanced case of suppurative parotitis (Fig. 1).

An US examination of the swelling will reveal the abscess. the
usual fluctuation may not be elicited due to the dense fibrous
capsule (derived from investing layer of deep cervical fascia)
of the parotid gland.
„

differential diagnoses

Figures 2A and B show contrast CT scan left parotid abscess.

treatment
„

„

w
fig. 1: Left side parotid abscess. 57 year-old-male diabetic irradiated patient of right side carcinoma tonsil. Patient had painful
swelling that reduced in size with antibiotics and abscess got
localized

b

figs 2a and b: Contrast CT scan left parotid abscess. Coronal images show peripherally enhancing hypodense lesion in left parotid gland
Source: Dr Swati Shah, Professor, Radiodiagnosis, GCR Medical College, Ahmedabad

disorders of Salivary glands

a

chapter 36

Incision and drainage: In addition to the treatment of acute
parotitis abscess needs incision and drainage. It is done
under the cover of antibiotics. An anterior based facial flap

treatment
It begins with aggressive medical treatment and includes:
Prompt fluid and electrolyte replacement, oral hygiene,
reversal of salivary stasis and antimicrobial therapy.
„ Salivary flow should be stimulated by sialogogues such as

lemon drops and orange juice.
„ Regular external and bimanual massage, starting from the
distal bed of the gland and working in the direction of duct
drainage helps greatly in drainage.
„ Analgesics and local heat application alleviate discomfort.
„ Antimicrobial therapy, which might need change after the
culture results, should be continued for 1 week after resolution of symptoms. Antibiotics include augmented penicillin
(Beta-lactamase producing bacteria in 75% cases) and
antistaphylococcal penicillin or a first-generation cephalosporin, vancomycin or linezolid (for methicillin-resistant S.
aureus infection) and metronidazole (for anaerobes).
„ Surgical drainage of a loculated abscess is done if conservative measures fail.

389